Cardiovascular 2

Question 1

congestive heart failure definition

Answer 1

chf is failure of the heart to pump an adequate amt of blood to supply the metabolic requirements of the organs. chf may be due to pathologic conditions inside or outside the heart

Question 2

chf epidemiology

Answer 2

affects nearly 5 million people in the US annually- contributes to 300000 deaths

Question 3

what are the compensatory mechanisms

Answer 3

activation of neurohumoral systems- release of norepinephrine with increased heart rate and contractility
activation of renin-angiotensin system with water/salt retention- increased circulatory volume
frank starling mechanism- increased end-diastolic filling volume stretches cardiac muscle fibers. at first the fibers contract more forcefully increasing cardiac output (compensated heart failure) but eventually they cannot keep up (Decompensated heart failure)
myocardial hypertrophy- increase in muscle fiber size, resulting in increased thickness of the ventricular wall but without increase in the size of the lumen

Question 4

does compensatory mechanisms work?

Answer 4

usually fail due to increased oxygen requirements of myocardium but without increased capillary supply- resulting in susceptibility to ischemia

Question 5

etiology of chf

Answer 5

ischemic heart disease
hypertension
myocarditis
cardiomyopathy
valvular disease

Question 6

what are the causes of right sided heart failure

Answer 6

left sided heart failure
subsequent pulmonary congestion leads to increased pulmonary arterial pressure
pulmonary hypertension (cor pulmonale)
valve disease
septal defects with left to right shunts

Question 7

manifestations of chf

right ventricular failure

Answer 7

congestion of liver (zonal or nutmeg pattern) and spleen

edema of subcutaneous tissue (feet and ankles)

Question 8

manifestations of chf

left ventricular failure

Answer 8

pulmonary edema and congestion, resulting in dyspnea, chronic cough, orthopnea

Question 9

manifestations of chf

left and/or right ventricular failure

Answer 9

cerebral hypoxia

chf due to left ventricular failure eventually leads to right ventricular failure

Question 10

congenital heart disease definition

Answer 10

congenital heart diseases may be caused by chromosomal anomalies or environmental factors
divided into cyanotic and noncyanotic forms
cyanotic forms generally have shunting of poorly-oxygenated systemic venous return to systemic arterial circulation, bypassing the lungs.
congenital heart disease include shunts (abnormal communication between chambers), abnormal connections between chambers and blood vessels, and absence of normal connections

Question 11

epidemiology of congenital heart disease

Answer 11

6-8/1000 live births in the US-

Question 12

causes of congenital heart disease

Answer 12

environmental factors (eg congenital rubella, maternal diabetes)
chromosomal abnormalities
90% are unknown and likely multifactorial

Question 13

common examples of noncyanotic

Answer 13

atrial septal defect- allows shunting between the atria- 2nd most common congenital malformation
ventricular septal defect- allows shunting between the ventricles- most common of cardiac malformations- 4/1000 live births
patent ductus arteriosus- this should close within a few days after birth and connects the aorta and pulmonary artery

Question 14

common examples of cyanotic

Answer 14

tetralogy of fallot- 4 anomalies include- ventricular septal defect, narrowing of right ventricular outflow, overriding of the aorta over vsd, right ventricular hypertrophy

transposition of the great arteries- the right ventricle empties into the aorta, the left ventricle empties into the pulmonary artery

Question 15

ischemic heart disease (IHD) definition

Answer 15

group of related disorders that are all characterized by imbalance between myocardial blood supply and myocardial oxygen demand (ischemia)
primarily (>90%) due to coronary artery atherosclerosis (coronary artery disease)

Question 16

ischemic heart disease epidemiology

Answer 16

leading cause of death in US- 500000 annually

Question 17

pathogenesis of ischemic heart disease

Answer 17

narrowing of coronary arteries (usually at least 75%) by atherosclerosis
gradual narrowing may lead to opening of collateral arteries
coronary artery thrombosis initiated by fissure in the fibrous cap of an atherosclerotic plaque
other factors- increased myocardial oxygen demand (hypertension), diminished blood volume (hypotension/shock), reduced oxygenation (pneumonia, CHF), reduced oxygen-carrying capacity (anemia)

Question 18

types of IHD

Answer 18

angina pectoris-
acute myocardial infarction
chronic IHD with CHF
sudden cardiac death

Question 19

angina pectoris

Answer 19

intermittent chest pain caused by transient reversible myocardial ischemia
chest pain of several minutes duration usually associated with exercise or emotional stress and relieved by rest
no myocardial necrosis occurs. in unstable angina- episodes of chest pain become more frequent and pain becomes more severe- longer lasting than stable angina- often precedes more serious ischemia or MI
stable angina- occurs predictably at certain levels of exertion- crushing or squeezing substernal pain that may radiate down the left arm or jaw (referred pain) relieved by rest or sublingual nitroglycerin (vasodilator to increase coronary perfusion)

Question 20

acute myocardial infarction

Answer 20

necrosis of cardiac muscle caused by ischemia
acute coronary artery thrombosis secondary to artherosclerosis
1.5 mil MI annually in US 1/3 die
severe ischemia lasting longer than 20-40 mins will cause irreversible myocyte injury and cell death
myocardial ischemia also contributes to arrhythmias probably because ischemic regions cause electrical instability (irritability)- may lead to ventricular fibrillation

Question 21

clinical presentation of MI

Answer 21

chest pain, shortness of breath, nausea/vomiting, diaphoresis, low grade fever

Question 22

what diagnostic tests for MI

Answer 22

ECG changes
elevation of serum enzymes (creatine kinase; ck-mb) and troponin derived necrotic myocytes
MI less than 12 hr old are usually not grossly apparent at autopsy
at 12-24 hours, infarcted area appears reddish blue

Question 23

pathology of MI

Answer 23

coagulation necrosis (few hours)
neutrophil infiltration (few days)
granulation tissue (1 week)
scar formation (wk-mos)

Question 24

treatment of MI

Answer 24

stents to open the coronary arteries clogged by artherosclerotic plaques
coronary artery by pass grafts (CABG) or clot busting drugs such as tissue plasminogen activator (TPA/streptokinase
reperfusion injury is a risk of these treatments

Question 25

complications of MI

Answer 25

arrhythmia and sudden death
CHF/shock
mural thrombus/emboli
myocardial rupture
mitral valve regurgitation
ventricular aneurysm
infarct expansion to involve right ventricle
chronic ischemic heart disease

Question 26

chronic ischemic heart disease

Answer 26

progressive heart failure due to ischemic myocardial damage
usually a history of MI
arrhythmia, CHF and subsequent MI lead to many deaths

Question 27

chronic IHD with CHF

Answer 27

progressive cardiac decompensation following acute MI or secondary to smaller ischemic events with eventual mechanical pump

Question 28

sudden cardiac death

Answer 28

sudden onset of ischemia-induced cardiac arrhythmia with or without myocardial necrosis (infarction)
this may occur in individuals with or without a previous history of IHD - most common cause is IHD (80-90%)
younger patients- congenital coronary artery abnormalities, aortic valve stenosis; mitral valve prolapse; myocarditis; dilated or hypertrophic cardiomyopathy; pulmonary hypertension; myocardial hypertrophy

Question 29

cardiomyopathy classfication

Answer 29

primary- the disease is solely or predominantly confined to the heart muscle
secondary- the heart is involved as part of a multisystem disorder
three morphologic patterns of cardiomyopathy: dilated, hypertrophic and restrictive

Question 30

dilated cardiomyopathy

Answer 30

heterogenous group of cardiac diseases which may be primary or secondary, genetic or acquired
hereditary basis in 20-50% of cases- related to alcoholism, myocarditis (viral?), pregnancy
dilation of all 4 heart chambers
histology shows variable fibrosis and myocyte hypertrophy
poor ventricular contractility (systolic dysfunction)

Question 31

hypertrophic cardiomyopathy

Answer 31

primary genetic cardiomyopathy
missense point mutation in one of several sarcomeric gene loci
disorder of sarcomeric proteins (myosin, myosin binding protein C, troponin T)
inherited as autosomal dominant with variable expression
inappropriate (spontaneous) myocardial hypertrophy, asymmetric hypertrophy which is greater in the interventricular septum than the left ventricular free wall and often obstructs the left ventricular outflow tract
stiff ventricles prevent adequate filling (diastolic dysfunction)
characteristic histology is disarray of cardiac myocytes and fibrosis

Question 32

restrictive cardiomyopathy

Answer 32

decrease in ventricular compliance (walll is stiffer) resulting in impaired ventricular filling during diastole
can be idiopathic or associated with other conditions that happen to affect the myocardium, such as radiation fibrosis, amyloidosis, hemochromatosis, and sarcoidosis

Question 33

myocarditis etiology

Answer 33

inflammation involving the myocardium
pyogenic bacteria: abscesses
viruses: interstitial mononuclear inflammatory cells with myocyte necrosis (coxsackie A and B)
parasites: in individual myocytes or interstitium with adjacent inflammation (chagas disease in s america)
hypersensitivity: often to drugs,perivascular inflammation with eosinophils
most common cause in the united states is viral infection
in some cases the etiology is unknown

Question 34

pathology of myocarditis

Answer 34

viral infection produces a lymphocytic infiltrate with foci of necrosis
pyogenic bacteria cause abscesses
parasites (such as trypanosomes in chagas disease- found in south america) infect individual myocytes or are in interstitial areas with surrounding inflammatory cells
hypersentivity (usually to drugs) causes a perivascular inflammatory infiltrate with many eosinophils